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The transcriptome analysis of C3H10T1/2 mesenchymal stem cells its derivatives expressing shRNA against NFIB or MLL1 during osteogenic differentiation

ABSTRACT: The transcriptome analysis of C3H10T1/2 mesenchymal stem cells its derivatives expressing shRNA against NFIB or MLL1 during osteogenic differentiation

PROVIDER: PRJNA945472 | ENA |

REPOSITORIES: ENA

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The transcriptome analysis of C3H10T1/2 mesenchymal stem cells its derivatives expressing shRNA against NFIB or MLL1 during osteogenic differentiation

Project description:To examine the impact of the NFIB/MLL1 complex on the transcriptome of C3H10T1/2 mesenchymal stem cells (MSCs) and to identify NFIB/MLL1-dependent genes during osteogenic differentiation, we performed RNA-sequencing (RNA-seq) analysis of six different samples at two time points.

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Genome-wide map of NFIB/MLL1 complex binding and H3K4me3 deposition during osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:To explore direct targets of NFIB/MLL1 complex and to examine the role of NFIB/MLL1 complex in genome-wide deposition of histone H3-K4 tri-methylation (H3K4me3), we conducted chromatin immunoprecipitation (ChIP) followed by deep sequencing (ChIP-seq) analysis of six different samples at two time points.

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Genome-wide map of NFIB/MLL1 complex binding and H3K4me3 deposition during osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

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NFIB/MLL1 complex is required for the stemness and the Dlx5-dependent osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

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Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:To investigate the cooperative function KDM4D/NFIB/MLL1 complex in the regulation of adipogenic differentiation, we established 10T1/2 cell lines in which each target gene has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

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Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

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Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

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Histone demethylase KDM4D cooperates with NFIB and MLL1 complex to regulate adipogenic differentiation of C3H10T1/2 mesenchymal stem cells.

Project description:The coordinated and sequential actions of lineage-specific transcription factors and epigenetic regulators are essential for the initiation and maintenance of cellular differentiation. We here report KDM4D histone demethylase as a key regulator of adipogenesis in C3H10T1/2 mesenchymal stem cells. The depletion of KDM4D results in impaired differentiation, which can be rescued by exogenous KDM4D, PPAR?, and C/EBP?, but not by C/EBP?. In addition, KDM4D interacts physically and functionally with both NFIB and MLL1 complex to regulate C/EBP? and PPAR? expression upon adipogenic hormonal induction. Although KDM4D is dispensable for the binding of both NFIB and MLL1 complex to the target promoters, the demethylation of tri-methylated H3K9 by KDM4D is required for NFIB and MLL1 complex to deposit tri-methylated H3K4 and activate PPAR? and C/EBP? expression. Taken together, our data provide a molecular framework for lineage-specific transcription factor and histone modifiers to cooperate in adipogenic differentiation, in which KDM4D removes repressive histone marks at genes with a bivalent chromatin domain and allows NFIB and MLL1 complex to promote the expression of key adipogenic regulators.

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